Dentists play an important role in the diagnosis and management of desquamative gingivitis. The importance of being able to recognise and properly diagnose this condition is accentuated by the fact that a serious and life threatening disease may initially manifest as desquamative gingivitis.
4. The International workshop for classification of
periodontal diseases and conditions noted that the
periodontist may be called upon to manage non-
plaque related mucocutaneous disorders either
alone or as a part of treatment team consisting of
physicians, dentists or other allied health care
professionals.
5. Chronic desquamative gingivitis is characterized by
intense redness and desquamation of the surface
epithelium of the attached gingiva.
Clinical features of desquamative gingivitis vary in
severity
Mild form
Moderate form
Severe form
7. Moderate form:
Patchy distribution of bright red
and gray areas involving marginal
and attached gingiva
Smooth and shiny.
Slight pitting with pressure
Massaging of the gingiva with the
finger results in peeling of the
epithelium and exposure of the
bleeding connective tissue
Occurs in 30 and 40 years of age
8. Severe form:
Wide areas of the oral
cavity involved
Surface epithelium
appears shredded
Blowing of air causes a
bubble in gingival
epithelium
Very painful
Constant dry, burning
sensation
13. Pathogenesis:
Current data suggest that OLP is a T cell-mediated
autoimmune disease in which auto-cytotoxic CD8+
T cells trigger apoptosis of oral epithelial cells.
However, the precise cause of OLP is unknown.
14. The skin lesions of OLP appear as small , angular,
flat topped papules.
15. Oral lichen planus presents as white striations , white
papules, white plaques, erythema, erosions or blisters
Present in a variety of forms:
RETICULAR
ATROPHIC,
PAPULAR,
ULCERATIVE
BULLOUS FORMS.
17. Plaque like lichen planus:
Slightly raised or flat
white area on the oral
mucous membranes.
Plaque type lesions may
clinically similar to
homogenous leukoplakia.
18. VESICULAR OR BULLOUS LESIONS
These lesions are uncommon & short lived on
the gingiva, quickly rupturing and leaving an
ulceration.
ATROPHIC LESIONS
Atrophy of the gingival tissues
with ensuing epithelial
thinning results in erythema
confined to the gingiva.
19.
20. DI- Linear-fibrillar deposits of fibrin in the basement
membrane zone.
Scattered immunoglobulin-staining cytoid bodies in
the upper areas of the lamina propria.
Serum tests using indirect immunofluorescence are
negative in lichen planus.
22. The keratotic lesions of oral lichen planus are
asymptomatic and do not require treatment.
The erosive, bullous, or ulcerative lesions of oral lichen
planus are treated with high-potency topical steroid
such as 0.05% fluocinonide ointment (three times
daily).
It can also be mixed 1:1 with carboxymethyl cellulose
(Orabase) paste or other adhesive ointment.
23. SEVERE CASES- Intralesional injections of
triamcinolone acetonide (10 to 20 mg) or short-term
regimens of 40 mg prednisone daily for 5 days followed
by 10 to 20 mg daily for an additional 2 weeks.
Anti fungal therapy.
24. Hippocrates was the first to describe pemphigoid as a
type of fever accompanied by blisters .
Types of pemphigoid that are as follows:
Bullous pemphigoid
Cicatrical / mucous membrane pemphigoid
Antiepiligrin pemphigoid
25. Cicatricial pemphigoid.
Chronic, vesiculobullous autoimmune disorder
It predominantly affects women in fifth decade of life.
The percentage of involvement is:
oral mucosal bullous lesion: 85-90%
occularlesions:66%,
nasal lesions: 15-23%,
laryngeal involvement;8-21%
26. The two major antigenic determinants for cicatricial
pemphigoid are bullous pemphigoid 1 and 2 (BP1 and
BP2).
Most cases of Cicatricial pemphigoid are the result of
an immune response directed against BP2 and less
commonly against BP1 and epiligrin
27. EXTRAORAL LESIONS :
Nasopharyngeal involvement is
characterized by rupture of vesicles in nasal
mucosa.
Dysphagia.
Dyspnea and laryngeal stenosis.
33. Localized lesions - Fluocinonide (0.05%) and
clobetasol propionate (0.05%) in an adhesive vehicle
can be used three times a day for up to 6 months.
If ocular involvement exists, systemic
corticosteroids are indicated.
When lesions do not respond to steroids, systemic
Dapsone (4-4'diaminodiphenylsulfone) has proven
to be effective
34. SEVERE CASES –
Intravenous immunoglobulins are another effective
but expensive treatment option in high-risk
patients.
37. No evidence of
acantholysis.
Developing vesicles are
subepithelial rather than
intraepithelial.
The epithelium separates
from the underlying
connective tissue at the
basement membrane zone.
38. IgG&C3 immune deposits along epithelial basement
membrane and circulating IgG antibodies to the
epithelial basement membrane.
Direct immunofluorescence is positive in 90% to
100% of these patients, whereas indirect
immunofluorescence is positive in 40% to 70% of
affected patients
39. The primary treatment is a moderate dose of
systemic prednisone.
Steroidsparing strategies (prednisone plus other
immunomodulator drugs) are used when high doses
of steroids are needed or the steroid alone fails to
control the disease .
For localized lesions of bullous pemphigoid,
highpotency topical steroids or tetracycline with or
without nicotinamide can be effective .
40. Derived from Greek word pemphix ( bubble or blister)
Pemphigus vulgaris is most common of pemphigus
diseases, which also includes
P.foliaceous
P.vegetens
P.erythematosus
41. Circulating autoantibodies are responsible for
disruption of intercellular junctions and loss of cell-
to-cell adhesion.
48. Painful, solitary small blisters and erosions with
surrounding erythema are present mainly on the
gingiva and the lateral border of the tongue. The hard
palate may also present similar lesions.
HISTOPATHOLOGY
Hyperkeratosis, acanthosis and liquefaction of the
basal cell layer with areas of sub epithelial clefting. The
underlying lamina propria exhibits a lymphohistocytic
chronic infiltrate in a band like configuration.
49.
50. For mild cases, topical steroids (Fluocinonide,
Clobetasol Propionate) and topical tetracycline may
produce clinical improvement.
SEVERE CASES- Hydrochloroquinine sulfate at a
dosage of 200-400mg/day
51. Is an uncommon mucocutaneous disorder with
predilection in women It clinically presents as a
pruritic vesiculobullous rash during middle to late
age.
ORAL LESIONS:
52. HISTOPATHOLOGY
Small, tense subepithelial bullae with
polymorphonuclear leukocyte infiltration as well as
large mononuclear cells are manifested. Similar to
those observed in erosive lichen planus.
IMMUNOFLUORESENCE
Linear deposits of IgA are
observed at the epithelial
connective tissue interface.
54. Combination of Sulfones and Dapsone.
Small amounts of Prednisone (10-30mg/day) can be
added.
Alternatively, tetracycline (2g/day) combined with
nicotinamide (1-5g/day) have shown promising results.
55. Chronic condition
Young adults (20-30 years)
Slight predilection for males.
Bilateral and symmetric pruritic papules/vesicles
Painful ulcerations preceded by collapse of ephemeral
vesicles/bullae.
56. HISTOPATHOLOGY
Focal aggregates of neutrophils and eosinophils
amidst deposits of fibrin at the apices of the dermal
pegs.
IMMUNOFLUORESENCE
Direct immunofluoresence show that IgA &C3 are
present at the dermal papillary apices. There is clear
association with celiac disease & circulatory anti
endomysial and anti gliaden antibodies may be of
diagnostic value.
58. It is an autoimmune disease with three different
clinical presentations
1. Systemic Lupus Erythematosus
2. Chronic Cutaneous Lupus Erythematosus
(CCLE)
3. Subacute Cutaneous Lupus Erythematosus
(SCLE)
59. Females 10 : 1
Affects kidneys, skin and
mucosa
Fever, weight loss and
arthritis
Rash on malar area
Oral lesions are present in
up to 40% of patients.
62. Cutaneous rashes are treated with topical steroids, sun
screens and hydroxy chloroquine.
For arthritis & mild pleuritis, NSAID’S or
hydroxychloroquine are used .
For severe systemic organ involvement moderate to
high doses of Prednisone are effective.
63. Factitious lesions
Graft vs. Host disease
Wegener's granulomatosis
Foreign body gingivitis
Kindler syndrome
64. In many cases of desquamative gingivitis it may not be
possible to determine the basic etiology. However, local
therapy together with deligence &patience will eventually
improve the condition and the etiologic background may
be discovered on the eventual appearance of other lesions
or symptoms.
It is clear that dentists play an important role in the
diagnosis and management of desquamative gingivitis. The
importance of being able to recognise and properly
diagnose this condition is accentuated by the fact that a
serious and life threatening disease may initially manifest
as desquamative gingivitis.
66. EricT. Stoopler et al, Desquamative gingivitis: Eariy
presenting symptom of mucocutaneous disease.
Quintessence Int 2003:34:582-586
L Lo Russo, R Guiglia,Effect of desquamative gingivitis on
periodontal status: a pilot study Oral Diseases 2010: 16:102–
107.
Lucio Lo Russo & Crescenzio Gallo Periodontal clinical and
microbiological data in desquamative gingivitis patients.
Clin Oral Invest 2014 18:917–925
AK.Markopoulos, D.Antoniades Desquamative gingivitis: A
clinical, histopathoiogic, and immunologic study.
Quintessence Int 1996:27:763-76.
Intially red in colour later reddish purple finally dirty brown colour
affecting predominantly the buccal mucosa, tongue and gingivae, although other sites are occasionally involved.
Characterized by fine white lines. That may form network but can also show circular pattern. Buccal mucosa most cmmnly affected site also appear on vermilion borders of lip.
Homogenous well demarcated white patch but not all surrounded by white striae .
Homogenous red area commonly seen in attached gingiva. It is not associated with striae.
Hyper keratosis , degeneration of basal keratinocytes, saw tooth rete pegs , band like sub epithelial mono nuclear infiltrate consisting of t cells and histiovytes.
Auto immune blistering disease that predominantly effects the mm including mouth oropharynx conjuctiva nasal and gentalia
As it is an auto immune blisterig disease associated with auto antibodies directed against basement membrane target antigen.
Ankyloblepharon(adhesion at the edges of the eyelids),
Mucosal lesiona are vesiculo bullous in nature relatively appears as thick walled persist for 24-48 hrs before rupturing and desquammating
Chiefly lymphocytes, plasma cells and eosinophils.
Reveled the Presence of Tissue bound basement membrane zone antibodies in most patients with this disease as well as circulating anti basement membrane zone antibodies in the serum of these pts.
Goal of the treatment is to supress blister formation to promote healind and prevent scarring.
Also called para pemphigus. It is characterized by presence of igG auto antibodies specific for bullous pemphigoid antigen BP230 and BP 180
Desquamate with minor trauma. Gingiva is very painful.
Basemmnt mebrane remains attached to ct rather than overlying seperated epithelium.
Because its etiologic factors are unknown, treatment of bullous pemphigoid is designed to control its signs and symptoms.
It is auto immune intra epithelial blistering disease affecting the skin and mucous membrane.
igG auto antibodies binds to cell surface keratinocyte molecues i.e., desmoglein 1 and 3
Which contains thin watery fluid that may become purulent ,nikolskys sign- loss of epi occasioned by rubbing apparently unaffected skin and it is caused by pre vesicular edema which disrupts dermal and epi dermal junctions.
Suprabasillar split ,
Direct immunofluorescence shows binding of IgG and C3 between epithelial cells, forming a “chicken wire” or “fish net” appearance.
Rare muco cutaneous disorder
a chronic subepidermal blistering disease that is associated with presence of linear deposits of IgA along the basement membrane zone characterized by pruritic vesiculobullous rash
Cutaneous manifestation of celiac disease.
Affects multiple organ systems through damage induced by circulating immunce complexes.
a.hyperkeratosis, acanthosis and intense lichenoid infiltrate b. basal layer destruction by the lichenoid infiltrate c. colloid body d.iflammatory infiltrate e. Blood vessels showing basement membrane thickening f. thickening of epithelial basement membrane (Immunoglobulin G